scholarly journals Shared genetic contributions to anxiety disorders and pathological gambling in a male population

2011 ◽  
Vol 132 (3) ◽  
pp. 406-412 ◽  
Author(s):  
Justine L. Giddens ◽  
Hong Xian ◽  
Jeffrey F. Scherrer ◽  
Seth A. Eisen ◽  
Marc N. Potenza
2005 ◽  
Vol 62 (9) ◽  
pp. 1015 ◽  
Author(s):  
Marc N. Potenza ◽  
Hong Xian ◽  
Kamini Shah ◽  
Jeffrey F. Scherrer ◽  
Seth A. Eisen

Author(s):  
Cheng Sun ◽  
Rita Spathis ◽  
Krithivasan Sankaranarayanan ◽  
Chim W. Chan ◽  
J. Koji Lum

The all-pervasive Internet has created serious problems, such as Internet overuse, which has triggered considerable debate over its relationship with addiction. To further explore its genetic susceptibilities and alternative explanations for Internet overuse, we proposed and evaluated four hypotheses, each based on existing knowledge of the biological bases of addiction, inattention, novelty-seeking, and harm-avoidance. Four genetic loci including DRD4 VNTR, DRD2 Taq1A, COMT Val158Met and 5-HTTLPR length polymorphisms were screened from seventy-three individuals. Our results showed that the DRD4 4R/4R individuals scored significantly higher than the 2R or 7R carriers in Internet Addiction Test (IAT). The 5-HTTLPR short/short males scored significantly higher in IAT than the long variant carriers. Bayesian analysis showed the most compatible hypothesis with the observed genetic results was based on attention (69.8%), whereas hypotheses based harm-avoidance (21.6%), novelty-seeking (7.8%) and addiction (0.9%) received little support. Our study suggests that carriers of alleles (DRD4 2R and 7R, 5-HTTLPR long) associated with inattentiveness are more likely to experience disrupted patterns and reduced durations of Internet use, protecting them from Internet overuse. Furthermore, our study suggests that Internet overuse should be categorized differently from addiction due to the lack of shared genetic contributions.


2014 ◽  
Vol 29 (5) ◽  
pp. 282-287 ◽  
Author(s):  
N. Carmiol ◽  
J.M. Peralta ◽  
L. Almasy ◽  
J. Contreras ◽  
A. Pacheco ◽  
...  

AbstractBipolar disorder and alcohol use disorder (AUD) have a high rate of comorbidity, more than 50% of individuals with bipolar disorder also receive a diagnosis of AUD in their lifetimes. Although both disorders are heritable, it is unclear if the same genetic factors mediate risk for bipolar disorder and AUD. We examined 733 Costa Rican individuals from 61 bipolar pedigrees. Based on a best estimate process, 32% of the sample met criteria for bipolar disorder, 17% had a lifetime AUD diagnosis, 32% met criteria for lifetime nicotine dependence, and 21% had an anxiety disorder. AUD, nicotine dependence and anxiety disorders were relatively more common among individuals with bipolar disorder than in their non-bipolar relatives. All illnesses were shown to be heritable and bipolar disorder was genetically correlated with AUD, nicotine dependence and anxiety disorders. The genetic correlation between bipolar and AUD remained when controlling for anxiety, suggesting that unique genetic factors influence the risk for comorbid bipolar and AUD independent of anxiety. Our findings provide evidence for shared genetic effects on bipolar disorder and AUD risk. Demonstrating that common genetic factors influence these independent diagnostic constructs could help to refine our diagnostic nosology.


2020 ◽  
Vol 87 (9) ◽  
pp. S338
Author(s):  
Laura Germine ◽  
Caitlin Carey ◽  
Yunru Huang ◽  
Stella Aslibekyan ◽  
Jordan Smoller ◽  
...  

2012 ◽  
Vol 37 (10) ◽  
pp. 1176-1180 ◽  
Author(s):  
Kelly C. Young-Wolff ◽  
Kenneth S. Kendler ◽  
Carol A. Prescott

2007 ◽  
Vol 10 (1) ◽  
pp. 174-179 ◽  
Author(s):  
Hong Xian ◽  
Jeffrey F. Scherrer ◽  
Wendy S. Slutske ◽  
Kamini R. Shah ◽  
Rachel Volberg ◽  
...  

AbstractProblem (P) and pathological gambling (PG) symptoms wax and wane. Past symptoms are a risk for future symptoms even after controlling for familial influences. To address the genetic architecture of lifetime PG and current PG symptoms, we tested for common and unique genetic factors to lifetime PG symptoms at baseline and past year PG symptoms at 10-year follow-up. Diagnostic and Statistical Manual of Mental Disorders (3rd ed., Rev.; DSM-III-R; American Psychiatric Association, 1987) lifetime criteria of one or more PG symptoms were derived in 1992 and past year PG symptoms in 2002 from 1675 individual twins from the Vietnam Era Twin Registry. Cholesky decomposition models were fit to baseline and past year PG symptoms. Under the best fitting model we observed that 49% of the risk for one or more baseline PG symptoms in 1992 was due to a genetic factor and 51% of the risk was due to a unique environmental factor. All of the genetic variance (57.5%) in risk to past year PG symptoms in 2002 was common with baseline PG symptoms. Unique environment accounted for the remaining variance in past year PG symptoms with 13% common to baseline and 30% specific to past year PG symptoms. The genetic contributions to lifetime and past year gambling symptoms 10 years later are similar. There is no evidence for genetic contributions unique to past year PG symptoms. However, most of the unique environmental influences to past year PG are not shared with lifetime PG. This may reflect the changed social–cultural environment between 1992 and 2002, characterized by increasing access to legalized gambling.


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